Evidence map›Paper›PMID 38530117›Full record

ArticleMolecular cancer therapeutics2024

Ultrasensitive Response Explains the Benefit of Combination Chemotherapy Despite Drug Antagonism.

Sarah C Patterson, Amy E Pomeroy, Adam C Palmer

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Sarah C PattersonDepartment of Pharmacology, Computational Medicine Program, UNC Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.ORCID 0000-0002-1393-895X
Amy E PomeroyDepartment of Pharmacology, Computational Medicine Program, UNC Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.ORCID 0000-0001-9217-3539
Adam C PalmerDepartment of Pharmacology, Computational Medicine Program, UNC Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.ORCID 0000-0001-5028-7028
University of North Carolina at Chapel Hill · US

Funding

SEEDING POSTDOCTORAL INNOVATORS IN RESEARCH &EDUCATIONK12GM000678 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DONALD T LYSLE, Kathryn Joanna Reissner · 1999 to 2026
$30.9M
Predoctoral Training in the Pharmacological SciencesT32GM135095 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Joseph Mauro Calabrese, Michael James Emanuele · 2020 to 2026
$3.6M
National Institute of General Medical Sciences (NIGMS) K12-GM000678National Institute of General Medical Sciences (NIGMS) T32-GM135095NIGMS NIH HHS K12 GM000678NIGMS NIH HHS T32 GM135095V Foundation for Cancer Research (VFCR) V2020-010
6 · The paper itself

Abstract

Most aggressive lymphomas are treated with combination chemotherapy, commonly as multiple cycles of concurrent drug administration. Concurrent administration is in theory optimal when combination therapies have synergistic (more than additive) drug interactions. We investigated pharmacodynamic interactions in the standard 4-drug "CHOP" regimen in peripheral T-cell lymphoma (PTCL) cell lines and found that CHOP consistently exhibits antagonism and not synergy. We tested whether staggered treatment schedules could improve tumor cell kill by avoiding antagonism, using in vitro models of concurrent or staggered treatments. Surprisingly, we observed that tumor cell kill is maximized by concurrent drug administration despite antagonistic drug-drug interactions. We propose that an ultrasensitive dose response, as described in radiology by the linear-quadratic (LQ) model, can reconcile these seemingly contradictory experimental observations. The LQ model describes the relationship between cell survival and dose, and in radiology has identified scenarios favoring hypofractionated radiotherapy-the administration of fewer large doses rather than multiple smaller doses. Specifically, hypofractionated treatment can be favored when cells require an accumulation of DNA damage, rather than a "single hit," to die. By adapting the LQ model to combination chemotherapy and accounting for tumor heterogeneity, we find that tumor cell kill is maximized by concurrent administration of multiple drugs, even when chemotherapies have antagonistic interactions. Thus, our study identifies a new mechanism by which combination chemotherapy can be clinically beneficial that is not contingent on positive drug-drug interactions.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsCyclophosphamideDoxorubicinVincristineCell Line, TumorCell SurvivalDose-Response Relationship, DrugDrug AntagonismDrug SynergismHumansLymphoma, T-Cell, PeripheralPrednisoneCyclophosphamideDoxorubicinPrednisoneVincristine

Identifiers

PMID38530117
PMCPMC11219261
OpenAlexW4393181965

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.